Molecular regulation of ENaC in the process of recovery in permeability lung edema

点击翻译按钮获取中文摘要

Alveolar epithelial cells have the ability of transporting sodium ion into cells. Under normal conditions, that mechanism allows alveolar space to keep dry, and can protect the barrier between alveoli and capillaries. We confirmed that in hyperoxia-induced lung injury epithelia sodium channel (ENaC) was reduced not just in quantity but in function. In addition to that, gene and protein expression were upregulated by the treatment of glucocorticoidm, and the removal of alveolar fluid progressed via ENaC. Under normal condition, ENaC relates to the transport of water from alveolar spce into alveolar epithelia cells and maintain fluid-free state. It reports in the model of acute lung injury that ENaC is downregulated by endotoxin, proinflammatory cytokines, and that oxidative stress inhibits the glucocorticoid dependent transcription of ENaC. It is thought that reduction of gene expression and protein expression is the important role to play in the onset of acute lung injury. However, it has never been investigated the point ENaC in recovery from permeability lung edema. In this point, the research is original, and unique.